Patients who fall into the interstitial cystitis category typically have complaints of urgency, frequency, nocturia, as well as suprapubic and deep pelvic pain. The majority of these patients will demonstrate abnormalities in behavior of the urethral sphincter (high pressures, spasticity, dyssynergia, enhanced sensitivity) and/or pelvic floor when studied urodynamically. They will also have significant discomfort on pelvic exam to pressure applied to the pelvic striated musculature (i.e. especially the levator). There are thus problems with the somatic, and visceral tissues. Treatment of the disorder thus may need to address inflammation and dysfunction of both the pelvic floor striated muscles and the urinary bladder. It is plausible for the primary disorder to be driven by the peripheral nerves to both the pelvic striated musculature and the detrusor. The nerves controlling these tissues are the pudendal (via S2 and S3), the pelvic parasympathetics (via S3 and S4) and the pelvic sympathetics. (T12-L2). This research aims to explore the theory that development of the Interstitial cystitis/Pelvic Pain syndrome has a predominate neural base, possibly linked to a chronic inefficiency in pelvic striated muscle behavior. This study will evaluate the interstitial cystitis problem in the following manner: 1. The Mechanism by which neural stress, via a pseudorabies virus neural transport modal, can lead to inflammation in the urinary bladder 2. Evaluate the role of neuropeptides as mediators of inflammatory changes in sacral spinal cord, the bladder or pelvic striated muscle 3. Provide urodynamic documentation of the behavior relationship between the pelvic floor and bladder during the evolution of cystitis 4. Evaluate the effect of drugs - via drug delivery - on symptoms and histologically documented inflammation typical for the interstitial cystitis/pelvic pain syndrome(s).